Excess CD33 promotes late onset of Alzheimer's

Study funded by the NIH finds that too much CD33 appears to promote late-onset of Alzheimer's disease by preventing support cells from clearing out toxic plaques. The research concludes that medications that impede CD33 activity might help treat the disorder

Singapore: Scientists funded by the National Institutes of Health (NIH) have discovered a potential strategy for developing treatments to stem the progression process in Alzheimer's disease.

The research is based on unclogging removal of toxic debris that accumulates in patients' brains, by blocking activity of a little-known regulator protein called CD33.

The team found that over-expression of CD33 in support cells (called microglia) in brains of patients, who had late-onset Alzheimer's disease.

Dr Rudolph Tanzi, Massachusetts General Hospital and Harvard University, US, and a grantee of the NIH's National Institute of Mental Health (NIMH) and National Institute on Aging (NIA), said that, "Too much CD33 appears to promote late-onset of Alzheimer's disease by preventing support cells from clearing out toxic plaques, key risk factors for the disease. Future medications that impede CD33 activity in the brain might help prevent or treat the disorder."